A nurse is conducting a visit to a client who is receiving palliative care at home for dying. The client’s husband tells the nurse, "I know she needs to be with God. That is the best place for her now." The client is experiencing which stage of Kubler-Ross’ stages of grieving?

Choice A reason: Exploring past interests is therapeutic but does not directly address the immediate suicide risk implied by hopelessness. Depression’s serotonin deficit heightens amygdala-driven despair, and assessing suicidal ideation is critical to prioritize safety over general exploration of interests.

Choice B reason: Reassuring the patient about reasons to live is dismissive and risks alienating them. Hopelessness in depression reflects serotonin and prefrontal cortex dysregulation, and this response fails to assess suicide risk, missing critical amygdala-driven warning signs.

Choice C reason: Asking about suicidal thoughts directly assesses risk, critical in depression with low serotonin and heightened amygdala activity driving hopelessness. This prioritizes safety, engaging prefrontal cortex reflection to identify immediate danger and guide intervention, making it the most appropriate response.

Choice D reason: Encouraging hope is vague and does not assess suicide risk. Depression’s serotonin deficit and amygdala hyperactivity require direct evaluation of suicidal ideation, as hopelessness signals potential danger, making this response inadequate for ensuring patient safety.

Choice A reason: Olanzapine does not primarily increase serotonin or norepinephrine. It blocks dopamine D2 and serotonin 5-HT2 receptors, reducing hallucinations driven by mesolimbic dopamine excess in schizophrenia. Increasing monoamines would exacerbate psychosis, not alleviate it, making this mechanism incorrect.

Choice B reason: Olanzapine, an atypical antipsychotic, blocks dopamine D2 receptors in the mesolimbic pathway, reducing excessive dopamine signaling that causes hallucinations in schizophrenia. It also modulates serotonin 5-HT2 receptors, balancing limbic activity, making this the primary mechanism for controlling psychotic symptoms.

Choice C reason: Decreasing neurotransmitter breakdown enzymes is the mechanism of MAOIs, not olanzapine. Olanzapine’s dopamine and serotonin receptor blockade reduces psychotic symptoms, not enzyme activity, making this choice irrelevant to its antipsychotic action in schizophrenia.

Choice D reason: Olanzapine does not normalize serotonin, norepinephrine, and dopamine levels but blocks their receptors, particularly dopamine D2, to reduce hallucinations. Normalizing levels is not its mechanism, as schizophrenia involves dopamine hyperactivity, not deficiency, making this choice inaccurate.